The drug that’s on the tip of America’s tongue, Ecstasy, otherwise known as “e”, “XTC”, “Adam”, “The Love Drug” or “MDMA”, garners an oddly unbalanced reputation. Some say it’s lethal. Yet the buzz amongst ravers speaks to the harmlessness of the “empathy drug”.

Taking ecstasy is a little like Russian Roulette. Call it an “allergic” reaction. There are several documented reports of death by ecstasy at extremely low doses. These unpredictable fatalities have occurred in healthy, otherwise drug-free ecstasy users. Additionally, there are both short and long-term health consequences of the drug. Some of these effects emerge only when the user has a concomitant illness or takes certain medications, while others do not. Here’s the skinny on this dehydration dynamo known as MDMA or 3, 4 - methylenedioxymethamphetamine.

THEY ALL CAME FROM GERMANY, or What do Nina Hagen, Nietzsche, and XTC have in common?

It was 1914 when MDMA first hit the scene, shoulder to shoulder with the Ubermensch. Later, the little pill arrived on America’s doorstep, armed with a small beige suitcase and a Pentax camera. In the 1970s, Ecstasy applied for a job in Psychology. Hailed as the Gal Friday of early 1980s Psychotherapists, Ecstasy earned the unprecedented reputation as a helpful (but illegal) tool for psychoanalysis. Unable to admit that it has a problem, Ecstasy bolted out of the Psychoanalyst’s office and swaggered onto the dance floor, heralded as the best thing since the Iron Chef. Those who dipped into Ecstasy were guaranteed “sensory enhancement and distortion and illusions without overt hallucinations” (Schwartz & Miller, 1997). So, it was not long before Ecstasy grew famous for its ability to produce speedy psychedelic effects upon the ecstatic. But America’s love affair with MDMA abruptly ends here.

It became readily apparent that Ecstasy exacts an immediate toll. Yes, some users may enjoy the logorrhea associated with MDMA, but others may not. Undeniably, most Xers would concur that the combination of muscle spasms, muscle damage, uncontrollable jaw clenching, heart palpitations, fevers up to 107 degrees, kidney damage, liver damage, dehydration, and coma tends to create an unwholesome feeling. This is especially true when the Ecstatic winds up in either the Emergency Room, Intensive Care Unit, or alternately, the morgue. But wait, there’s more.

HEN’S TEETH IN THE HEPATOCYTES

Fatal liver damage means trouble of the messy kind. Because without your liver, you would slowly bleed to death internally as blood leaks out of the blood vessels and into the tissue spaces. It also means that you starve to death, because you cannot metabolize food without your liver. Meanwhile, your hungry pancreas digests itself alive. Worse still, you run the risk of strokes and heart failure. And a blown liver means that your skin turns yellows as your brain becomes unable to coordinate speech, movement and vital functions.

That is your introduction to the story of a 20 year old man who, “Six days before symptoms developed... took one Ecstasy tablet, proceeded into liver failure, became delirious, suffered acute renal failure, and acute pancreatitis.” (Schirren, Berghaus,& Sackmann)

This unfortunate individual with MDMA-induced liver damage then developed bleeding problems, including the bursting of his red blood cells, the destruction of his platelets and profuse nosebleeds. Luckily, the man survived, returning to health after four months.

To liven things up, a British Coroner joins in our tale. Dr. A. R. W. Forrest, Assistant Deputy Coroner of Sheffield, UK relates the potential for Disseminated Intravascular Coagulation (DIC) as a “hens-tooth rare” but potentially lethal side effect of ecstasy. Associated with liver damage, this bleeding disorder conjures up images of E-bola. Those afflicted with DIC hemorrhage internally and externally, even from the ears and hair follicles.

DEATH

Another unwanted side effect of Ecstasy is death. S. Gore reports in the highly reputed medical journal, The Lancet, that amongst 15-24 year old British, Ecstasy induced death rates are five times higher than those caused by car crashes. Likewise, Schwartz and Miller furnish proof of 53 Ecstasy related fatalities.

BIRTH DEFECTS & THE LOVE DRUG

The effects of Ecstasy upon a developing fetus are anything but lovely. Ecstasy proves itself to be the year 2000’s answer to thalidomide. In one report, Congenital Anomalies After Prenatal Ecstasy Exposure, McElhatton documents multiple types of Ecstasy related birth defects. These include deformities such as “absence of upper limbs, left scapula, & clavicles”, and the “left fourth toe underlying the third toe”. Just a few of the other problems associated with Ecstasy use during pregnancy include fetal heart disease, low birth weight, and high rates of both miscarriage and foot deformities.

THE PARTY THAT NEVER ENDS

XTC induced nervous system damage falls into overlapping categories, the temporary with the permanent. Today’s headings include dopaminergic neurotoxicity, serotonin neurotoxicity, excessive antidiuretic hormone release, and generalized neurotoxicity.

DOPAMINERGIC NEUROTOXICITY

Chemicals called neurotransmitters send messages from the brain to muscles, organs, tissues, and cells to maintain homeostasis. Different parts of the brain manufacture different chemicals. The substantia nigra, located in the brain’s basal ganglia, produces a neurotransmitter called dopamine. Dopamine “acts to provide a balance between inhibitory and excitatory actions” (Monahan, Drake, Neighbors, 1995). In other words, dopamine coordinates the invisible “stop” and “go” signals required for seamless motion. Now, envision XTC poisoning the substantia nigra, destroying its capability to synthesize dopamine correctly.

Scientists assert that Parkinson’s Disease results from degeneration of the substantia nigra, homefront of dopmaine synthesis. According to Monahan etal, symptoms of Parkinsons’s Disease include tremors, paralysis, drooling, facial expressionlessness, postural instability, gait incoordination, involuntarily bent arms, uncontrollable rigidity, difficulties with speech, inability to stop movements, and problems swallowing.
Mintzer, Hickenbottom, & Gilman explain how a 29 year old man developed Parkinsonism soon after taking Ecstasy. The man’s symptoms emerged as mere clumsiness, but soon deteriorated into serious gross motor dysfunction. Eventually, he lost the motor coordination to write and drive. Both his career and independence vanished, supplanted by the need for assisted living. Two months later, he could no longer blink, speak, or walk normally. The writers conclude that Ecstasy seriously damaged this man’s substantia nigra, resulting in the symptoms of Parkinson’s disease.

XTC & THE SEROTONIN SYNDROME - The empathetic serotomimetic

Whereas Ecstasy inhibits dopamine levels, scientists believe that the drug initially amplifies levels of serotonin. Serotonin, or 5-hydroxytryptamine, is a vasoconstictive chemical present throughout the body. It plays an important role in sensory perception and sleep patterns (Tabers, page 1784). According to Mueller & Korey, neurochemical studies conducted on lab animals reveal a twofold effect of Ecstasy upon serotonin activity. ‘Presynaptic juctions’ are spaces adjacent to nerve endings between communicating neurons. First, Ecstasy initiates the bombardment of presynaptic junctions with excess serotonin. Then, the drug interferes with serotonin’s reuptake. This type of alteration in serotonin activity can lead to a potentially lethal crises called Serotonin Syndrome.

Mueller & Korey characterize the Serotonin Syndrome as a set of symptoms including high fever, altered levels of consciousness, muscular rigidity, and autonomic instability. Autonomic instability can be life threatening because the autonomic nervous system regulates the cardiovascular, respiratory, digestive, genitourinary, thermoregulatory, adrenal, ocular and metabolic systems. So far, there is no cure for Serotonin Syndrome.
Mueller & Korey recount the downward spiral ending in the death of a 20 year old woman who died from Serotonin Syndrome after ingesting two XTC tablets, “Paramedics delivered the patient to the hospital by ambulance in critical condition. Except for the two XTC tablets, she had taken no medications and had no previous medical problems. She arrived on the unit cyanotic (blue), and unresponsive. Her temperature was 107 degrees, and her pulse 160 beats per minute. She developed critical heart problems, (ventricular fibrillation), had a grand-mal seizure, then lost her pulse. She received CPR, then suffered another seizure. Despite treatment with multiple life sustaining measures, her blood pressure became critically low, and she continued with cardiac problems (malignant dysrhythmias), until she died four hours after arrival."

EXCESSIVE ANTIDIURETIC HORMONE RELEASE IN XTC COMA

Antidiuretic hormone (ADH) is a neurochemical manufactured in the hypothalamus of the brain. Antidiuretic hormone elevates blood pressure and maintains fluid volume by preventing the excretion of urine. Some rave-goers drink extra fluids to avoid the dehydration associated with XTC induced hyperthermia. In the past, if ravers developed hyponatremia and cerebral edema (water on the brain), their water drinking was blamed as the cause.

New evidence proves that another mechanism, one related to XTC’s penchant for neurochemical alterations of the brain, places users at risk for cerebral edema and coma. Ecstasy releases wild quantities of antidiuretic hormone. The pathology of this neurochemical insult can not be overstated.

Too much antidiuretic hormone means too little urination, filling the body with fluid. In concert with extra water intake, excessive ADH production leads to water intoxication, stupor, coma, cerebral edema, and possible death.

Holden & Jackson report the clinical course of a regular Ecstasy user who had hitherto avoided serious untoward effects. Their article describes how a 20 year old woman became comatose after swallowing a single ecstasy pill with lots of water: Upon arrival at the hospital, her brain scan revealed cerebral edema. She was placed on a ventilator. Her antidiuretic hormone levels were critically high. She survived, “Two months later reporting flashbacks and anxiety symptoms”. Holden & Jackson state that antidiuretic hormone release associated with Ecstasy use “is the primary pathogenic mechanism” in this user’s ecstasy coma. Additionally, readers are admonished that ADH levels can remain elevated for some time after XTC ingestion, potentiating coma and death.

GENERAL NEUROLOGICAL DAMAGE

In general, as XTC travels through neurons of the brain, it degrades the axons that conduct impulses from one brain cell (neuron) to the next. If axons are the bridges between neurons, then XTC can be thought of as a fire, burning those bridges as it ignites a spectacle. The axon degeneration is thought to take two days for total completion (Molliver etal). Other studies have proven that MDMA causes “significant anatomical neurodegeneration (Mintzer etal)". In the short run, this might manifest as mere fuzziness. In the long run, this could translate into intractable “burnout”.

IMMUNOSUPPRESSION - Run for your lives little viruses, POP OUT OF YOUR HOMES!

Netsurfers posting on the web ask why, after taking XTC, do their shingles and herpes reemerge? Nicholas Saunders replies that sleep deprivation accompanying Ecstasy use reactivates pre-existing viruses.

It is plausible that the neurotoxic effects of XTC could contribute to the recurrence of herpes. Latent herpes viruses reside in the nerve ganglia (Tortora, Funke, Case). Given that XTC destroys nerve axons, latent viruses stored in a nervous system under siege might “jump ship”, seeking refuge in the bloodstream, to resurface as skin lesions (my theory).

DRUG INTERACTIONS

Do not take XTC. If you disobey this command and take XTC anyways, then please do not mix XTC with MAOI inhibitors, SSRI’s, ritonavir, viagra, decongestants, ephedrines, pseudoephedrines, phenylpropanalamine (diet pills), and asthma medications such as ventolin. This list is by no means comprehensive. These drug mixtures together can be fatal.

THE END OF ECSTASY

Its disco days over, our tight-lipped MDMA was last spotted at the barbershop for a trim of his disturbingly well-coifed black moustache. Close followers of the pill ruefully watched as he packed his beige suitcase full of notecards, hollered “Achtung, baby!” and took off to a deserted island where he could finally hook up with Lenny Bruce, and that other favorite....oh, what the hell was his name?

SAYS WHO?*

1. Gore, S. (1999, October). Fatal uncertainty:death-rate from use of ecstasy or heroine. The Lancet, 354

2. Holden,R. & Jackson, M. (1996, April). "Near Fatal Hyponatremic Coma Due to Vasopressin Over-Secretion After 'Ecstasy'" (3,4 - MDMA). The Lancet, 347, page 1052

3. McElhatton, P.R., Bateman, D.N., Evans, C., Pughe, K.R., Thomas, S.H.L. (1999, October). "Congenital Anomalies After Prenatal Ecstasy Exposure". The Lancet, 354 page 1441

4. McKenna, D.J. (1999) "MDMA Neurotoxicity: An Update" 1999 Hyperreal Drug Archives Snapshot

5. Mintzer, Hickenbottom, & Gilman (1999, October). "Parkinsonism After Taking Ecstasy" New England Journal of Medicine (340) 18. 1443

6. Monahan, F., Drake, T., Neighbors, M. (1994) Nursing Care of Adults Pennsylvania: Saunders. page 1513

7. Mueller, P. & Korey, W. (1998, September) "Death by 'Ecstasy': The Serotonin Syndrome" Annals of Emergency Medicine 32 (3) pp. 377-380.

8. Saunders, N. (http://ecstasy.org/)

9. Schirren, Berghaus, Sackmann. (1999, January). "Thrombotic Thrombocytopenic Purpura After Ecstasy Induced Acute Liver Failure" Annals of Internal Medicine 130 ( 2)

10. Schwartz, R.& Miller, N. (1997, October) "MDMA and the Rave: A Review" Pediatrics 100 (4) pp. 705-708.

11. Thomas, C. (1993). Taber’s Cyclopedic Medical Dictionary, F.A. Davis Co., Philadelphia.

* reference page title by Io Cyrus

© 2004 Jessica Faller Berger. All rights reserved. Any use of these files electronically or otherwise is strictly prohibited.